The expression of <i>Helicobacter pylori tfs</i> plasticity zone cluster is regulated by <scp>pH</scp> and adherence, and its composition is associated with differential gastric <scp>IL</scp>‐8 secretion

Silva, Bruno; Nunes, Baltazar; Vale, Filipa F.; Rocha, Raquel; Gomes, João Paulo; Dias, Ricardo; Oleastro, Mónica

doi:10.1111/hel.12390

Cited by 21 publications

(19 citation statements)

References 57 publications

(113 reference statements)

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“…They generally contain complete sets of genes required to produce T4SS protein, as well as genes encoding different DNA processing proteins . A complete T4SS plasticity zone cluster is known to be a virulence factor that may be important for the colonization of H. pylori- and development of severe outcomes of infection with cagA‐positive strains . Additionally, genes encoding T4SS proteins can be transferred by conjugation between Rhizobium radiobacter and Bartonella rattaustraliani .…”

Section: Discussionmentioning

confidence: 99%

Evaluation of gastric microbiome and metagenomic function in patients with intestinal metaplasia using 16S rRNA gene sequencing

Park

Lee

et al. 2018

Helicobacter

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Background Despite recent advances in studies on the gastric microbiome, the role of the non‐Helicobacter pylori gastric microbiome in gastric carcinogenesis remains unclear. We evaluated the characteristics of the gastric microbiome and metagenomic functions in patients with IM. Methods Participants were classified into six groups according to disease status (chronic superficial gastritis [CSG], intestinal metaplasia [IM], and cancer) and H. pylori‐ infection status (H. pylori‐positive and H. pylori‐negative). The gastric microbiome was analyzed in mucosal tissues at the gastric antrum by 16S rRNA gene sequencing. Moreover, we assessed the metagenome including the type IV secretion system (T4SS) gene, as T4SS proteins are essential for transferring CagA from H. pylori- into the human gastric epithelium. Results Among the 138 included patients, 48, 9, 23, 14, 12, and 32 were classified into the H. pylori‐negative CSG, H. pylori‐negative IM, H. pylori‐negative cancer, H. pylori‐positive CSG, H. pylori‐positive IM, and H. pylori‐positive cancer groups, respectively. Cyanobacteria were predominant in the H. pylori‐negative CSG group compared to in the H. pylori‐negative IM and H. pylori‐negative cancer groups (H. pylori‐negative CSG vs H. pylori‐negative IM vs H. pylori‐negative cancer: 14.0% vs 4.2% vs 0.04%, P < 0.001). In contrast, Rhizobiales were commonly observed in the H. pylori‐negative IM group (H. pylori‐negative CSG vs H. pylori‐negative IM vs H. pylori‐negative cancer: 1.9% vs 15.4% vs 2.8%, P < 0.001). The relative abundance of Rhizobiales increased as H. pylori‐infected stomachs progressed from gastritis to IM. In the H. pylori‐negative IM group, genes encoding T4SS were prevalent among the metagenome. Additionally, after H. pylori- eradication therapy, the gastric microbiome was similar to the microbiome observed after spontaneous clearance of H. pylori-. Conclusions The relative abundance of Rhizobiales was higher in patients with H. pylori‐negative IM than in those with H. pylori‐negative CSG or cancer. Additionally, T4SS genes were highly observed in the metagenome of patients with IM. Highly abundant T4SS proteins in these patients may promote gastric carcinogenesis.

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Section: Discussionmentioning

confidence: 99%

Evaluation of gastric microbiome and metagenomic function in patients with intestinal metaplasia using 16S rRNA gene sequencing

Park

Lee

et al. 2018

Helicobacter

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“…Analysis of the H. pylori TFSS plasticity zone cluster showed that the whole composition of TFSS in association with CagA positivity may induce higher IL‐8 during cell line co‐culture and was influenced by adherence and pH of infection . Lastly, a single operon was found to regulate the expression of its component spanning from VirB2 to VirB10 …”

Section: Virulence Factorsmentioning

confidence: 99%

“…25 Analysis of the H. pylori TFSS plasticity zone cluster showed that the whole composition of TFSS in association with CagA positivity may induce higher IL-8 during cell line co-culture and was influenced by adherence and pH of infection. 26 Lastly, a single operon was found to regulate the expression of its component spanning from VirB2 to VirB10. 26 27 While urease appeared to be less essential after established colonization, chronic infection was restored by a positive selection process that altered the repressor protein, supporting a continual requirement for urease.…”

Section: Non-cag Virulence Factorsmentioning

confidence: 99%

“…26 Lastly, a single operon was found to regulate the expression of its component spanning from VirB2 to VirB10. 26 27 While urease appeared to be less essential after established colonization, chronic infection was restored by a positive selection process that altered the repressor protein, supporting a continual requirement for urease. 27 This approach may be applied to other virulence factors for understanding their roles under certain conditions, in either in vitro or in vivo studies.…”

Section: Non-cag Virulence Factorsmentioning

confidence: 99%

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Pathogenesis of Helicobacter pylori infection

2018

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In this review, we highlight progress in the last year in characterizing known virulence factors like flagella and the Cag type IV secretion system with sophisticated structural and biochemical approaches to yield new insight on the assembly and functions of these critical virulence determinants. Several aspects of Helicobacter pylori physiology were newly explored this year and evaluated for their functions during stomach colonization, including a fascinating role for the essential protease HtrA in allowing access of H. pylori to the basolateral side of the gastric epithelium through cleavage of the tight junction protein E-cadherin to facilitate CagA delivery. Molecular biology tools standard in model bacteria, including regulated gene expression during animal infection and fluorescent reporter gene fusions, were newly applied to H. pylori to explore functions for urease beyond initial colonization and establish high salt consumption as a mediator of gene expression changes. New sequencing technologies enabled validation of long postulated roles for DNA methylation in regulating H. pylori gene expression. On the cell biology side, elegant work using lineage tracing in the murine model and organoid primary cell culture systems has provided new insights into how H. pylori manipulates gastric tissue functions, locally and at a distance, to promote its survival in the stomach and induce pathologic changes. Finally, new work has bolstered the case for genomic variation as an important mechanism to generate phenotypic diversity during changing environmental conditions in the context of diet manipulation in animal infection models and during human experimental infection after vaccination.

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“…All of the NUD and PUD H. pylori pediatric strains were genotyped for the presence/status of babA, babB, babC, cagA, vacAsallele, hopQ allele, oipA, sabA, hopZ, and homB outer membrane protein encoding genes (Table 1) by whole genome sequencing (WGS), considering the previously published 12 H. pylori genomes [44,45], and eight new genomes, that were sequenced on a MiSeq Illumina platform, as previously described [45]. Briefly, high-quality genomic DNA samples from pure bacterial cultures were used to prepare Nextera XT Illumina libraries that were sequenced on an Illumina MiSeq platform (Illumina Inc., San Diego, CA) using the v.2 (300 cycles, 2×150 nt reads or 500 cycles, 2×250 nt reads) kit, according to the manufacturer's instructions.…”

Section: Genotyping Of H Pylori Virulence Genesmentioning

confidence: 99%

BabA-mediated adherence of pediatric ulcerogenic H. pylori strains to gastric mucins at neutral and acidic pH

et al. 2018

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2018)BabA-mediated adherence of pediatric ulcerogenic H.pylori strains to gastric mucins at neutral and acidic pH, ABSTRACT Helicobacter pylori infection can result in non-ulcer dyspepsia (NUD), peptic ulcer disease (PUD), adenocarcinoma, and gastric lymphoma. H. pylori reside within the gastric mucus layer, mainly composed of mucins carrying an array of glycan structures that can serve as bacterial adhesion epitopes. The aim of the present study was to characterize the binding ability, adhesion modes, and growth of H. pylori strains from pediatric patients with NUD and PUD to gastric mucins. Our results showed an increased adhesion capacity of pediatric PUD H. pylori strains to human and rhesus monkey gastric mucins compared to the NUD strains both at neutral and acidic pH, regardless if the mucins were positive for Lewis b (Le b ), Sialyl-Lewis x (SLe x ) or LacdiNAc. In addition to babA positive strains being more common among PUD associated strains, H. pylori babA positive strains bound more avidly to gastric mucins than NUD babA positive strains at acidic pH. Binding to Le b was higher among babA positive PUD H. pylori strains compared to NUD strains at neutral, but not acidic, pH. PUD derived babA-knockout mutants had attenuated binding to mucins and Le b at acidic and neutral pH, and to SLe x and DNA at acidic pH. The results highlight the role of BabA-mediated adherence of pediatric ulcerogenic H. pylori strains, and points to a role for BabA in adhesion to charged structures at acidic pH, separate from its specific blood group binding activity. ARTICLE HISTORY

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The expression of Helicobacter pylori tfs plasticity zone cluster is regulated by pH and adherence, and its composition is associated with differential gastric IL‐8 secretion

Abstract: A complete tfs plasticity zone cluster is a virulence factor that may be important for the colonization of H. pylori and to the development of severe outcomes of the infection with cagA-positive strains.

Cited by 21 publications

References 57 publications

Evaluation of gastric microbiome and metagenomic function in patients with intestinal metaplasia using 16S rRNA gene sequencing

Evaluation of gastric microbiome and metagenomic function in patients with intestinal metaplasia using 16S rRNA gene sequencing

Pathogenesis of Helicobacter pylori infection

BabA-mediated adherence of pediatric ulcerogenic H. pylori strains to gastric mucins at neutral and acidic pH

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